Analysis of the presynaptic action potential’s (AP_syn) role in synaptic facilitation in hippocampal pyramidal neurons has been difficult due to size limitations of axons. We overcame these size barriers by combining high-resolution optical recordings of membrane potential, exocytosis, and Ca²⁺ in cultured hippocampal neurons. These recordings revealed a critical and selective role for K_v1 channel inactivation in synaptic facilitation of excitatory hippocampal neurons. Presynaptic K_v1 channel inactivation was mediated by the K_vβ1 subunit and had a surprisingly rapid onset that was readily apparent even in brief physiological stimulation paradigms including paired-pulse stimulation. Genetic depletion of K_vβ1 blocked all broadening of the AP_syn during high-frequency stimulation and eliminated synaptic facilitation without altering the initial probability of vesicle release. Thus, using all quantitative optical measurements of presynaptic physiology, we reveal a critical role for presynaptic K_v channels in synaptic facilitation at presynaptic terminals of the hippocampus upstream of the exocytic machinery.

由于轴突的大小限制，很难分析海马锥体神经元突触促进中突触前动作电位（AP _syn）的作用。我们通过结合培养海马神经元中膜电位，胞吐作用和Ca ²⁺的高分辨率光学记录来克服这些尺寸障碍。这些记录揭示了K _v 1通道失活在兴奋性海马神经元的突触促进中的关键和选择性作用。突触前ķ _v 1通道的失活是由K个介导_v β1亚基和有一个令人惊讶的快速起效，即使在短暂是显而易见的生理刺激范例包括双脉冲刺激。钾的遗传消耗_v β1阻断AP的所有加宽_顺高频刺激期间和消除突触便利而不改变囊泡释放的初始概率。因此，使用突触前生理的所有定量光学测量，我们揭示了突触前K _v通道在外源性机器上游海马突触前末端的突触促进中的关键作用。